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What is Group Psychotherapy?

Introduction

Group psychotherapy, or group therapy, is a form of psychotherapy in which one or more therapists treat a small group of clients together as a group. The term can legitimately refer to any form of psychotherapy when delivered in a group format, including Art therapy, cognitive behavioural therapy or interpersonal therapy, but it is usually applied to psychodynamic group therapy where the group context and group process is explicitly utilised as a mechanism of change by developing, exploring and examining interpersonal relationships within the group.

The broader concept of group therapy can be taken to include any helping process that takes place in a group, including support groups, skills training groups (such as anger management, mindfulness, relaxation training or social skills training), and psychoeducation groups. The differences between psychodynamic groups, activity groups, support groups, problem-solving and psychoeducational groups have been discussed by psychiatrist Charles Montgomery. Other, more specialised forms of group therapy would include non-verbal expressive therapies such as art therapy, dance therapy, or music therapy.

Brief History

The founders of group psychotherapy in the USA were Joseph H. Pratt, Trigant Burrow and Paul Schilder. All three of them were active and working at the East Coast in the first half of the 20th century. In 1932 Jacob L. Moreno presented his work on group psychotherapy to the American Psychiatric Association, and co-authored a monograph on the subject. After World War II, group psychotherapy was further developed by Moreno, Samuel Slavson, Hyman Spotnitz, Irvin Yalom, and Lou Ormont. Yalom’s approach to group therapy has been very influential not only in the USA but across the world.

An early development in group therapy was the T-group or training group (sometimes also referred to as sensitivity-training group, human relations training group or encounter group), a form of group psychotherapy where participants (typically, between eight and 15 people) learn about themselves (and about small group processes in general) through their interaction with each other. They use feedback, problem solving, and role play to gain insights into themselves, others, and groups. It was pioneered in the mid-1940s by Kurt Lewin and Carl Rogers and his colleagues as a method of learning about human behaviour in what became the National Training Laboratories (also known as the NTL Institute) that was created by the Office of Naval Research and the National Education Association in Bethel, Maine, in 1947.

Moreno developed a specific and highly structured form of group therapy known as psychodrama (although the entry on psychodrama claims it is not a form of group therapy). Another recent development in the theory and method of group psychotherapy based on an integration of systems thinking is Yvonne Agazarian’s systems-centred therapy (SCT), which sees groups functioning within the principles of system dynamics. Her method of “functional subgrouping” introduces a method of organizing group communication so it is less likely to react counterproductively to differences. SCT also emphasizes the need to recognise the phases of group development and the defences related to each phase in order to best make sense and influence group dynamics.

In the United Kingdom group psychotherapy initially developed independently, with pioneers S. H. Foulkes and Wilfred Bion using group therapy as an approach to treating combat fatigue in the Second World War. Foulkes and Bion were psychoanalysts and incorporated psychoanalysis into group therapy by recognising that transference can arise not only between group members and the therapist but also among group members. Furthermore, the psychoanalytic concept of the unconscious was extended with a recognition of a group unconscious, in which the unconscious processes of group members could be acted out in the form of irrational processes in group sessions. Foulkes developed the model known as group analysis and the Institute of Group Analysis, while Bion was influential in the development of group therapy at the Tavistock Clinic.

Bion’s approach is comparable to social therapy, first developed in the United States in the late 1970s by Lois Holzman and Fred Newman, which is a group therapy in which practitioners relate to the group, not its individuals, as the fundamental unit of development. The task of the group is to “build the group” rather than focus on problem solving or “fixing” individuals.

In Argentina an independent school of group analysis stemmed from the work and teachings of Swiss-born Argentine psychoanalyst Enrique Pichon-Rivière. This thinker conceived of a group-centred approach which, although not directly influenced by Foulkes’ work, was fully compatible with it.

Therapeutic Principles

Irvin Yalom proposed a number of therapeutic factors (originally termed curative factors but renamed therapeutic factors in the 5th edition of The Theory and Practice of Group Psychotherapy).

  • Universality:
    • The recognition of shared experiences and feelings among group members and that these may be widespread or universal human concerns, serves to remove a group member’s sense of isolation, validate their experiences, and raise self-esteem
  • Altruism:
    • The group is a place where members can help each other, and the experience of being able to give something to another person can lift the member’s self esteem and help develop more adaptive coping styles and interpersonal skills.
  • Instillation of hope:
    • In a mixed group that has members at various stages of development or recovery, a member can be inspired and encouraged by another member who has overcome the problems with which they are still struggling.
  • Imparting information:
    • While this is not strictly speaking a psychotherapeutic process, members often report that it has been very helpful to learn factual information from other members in the group.
    • For example, about their treatment or about access to services.
  • Corrective recapitulation of the primary family experience:
    • Members often unconsciously identify the group therapist and other group members with their own parents and siblings in a process that is a form of transference specific to group psychotherapy.
    • The therapist’s interpretations can help group members gain understanding of the impact of childhood experiences on their personality, and they may learn to avoid unconsciously repeating unhelpful past interactive patterns in present-day relationships.
  • Development of socialising techniques:
    • The group setting provides a safe and supportive environment for members to take risks by extending their repertoire of interpersonal behaviour and improving their social skills
  • Imitative behaviour:
    • One way in which group members can develop social skills is through a modelling process, observing and imitating the therapist and other group members.
    • For example, sharing personal feelings, showing concern, and supporting others.
  • Cohesiveness:
    • It has been suggested that this is the primary therapeutic factor from which all others flow. Humans are herd animals with an instinctive need to belong to groups, and personal development can only take place in an interpersonal context.
    • A cohesive group is one in which all members feel a sense of belonging, acceptance, and validation.
  • Existential factors:
    • Learning that one has to take responsibility for one’s own life and the consequences of one’s decisions.
  • Catharsis:
    • Catharsis is the experience of relief from emotional distress through the free and uninhibited expression of emotion.
    • When members tell their story to a supportive audience, they can obtain relief from chronic feelings of shame and guilt.
  • Interpersonal learning:
    • Group members achieve a greater level of self-awareness through the process of interacting with others in the group, who give feedback on the member’s behaviour and impact on others.
  • Self-understanding:
    • This factor overlaps with interpersonal learning but refers to the achievement of greater levels of insight into the genesis of one’s problems and the unconscious motivations that underlie one’s behaviour.

Settings

Group therapy can form part of the therapeutic milieu of a psychiatric in-patient unit or ambulatory psychiatric partial hospitalisation (also known as day hospital treatment). In addition to classical “talking” therapy, group therapy in an institutional setting can also include group-based expressive therapies such as drama therapy, psychodrama, art therapy, and non-verbal types of therapy such as music therapy and dance/movement therapy.

Group psychotherapy is a key component of milieu therapy in a therapeutic community. The total environment or milieu is regarded as the medium of therapy, all interactions and activities regarded as potentially therapeutic and are subject to exploration and interpretation, and are explored in daily or weekly community meetings. However, interactions between the culture of group psychotherapeutic settings and the more managerial norms of external authorities may create ‘organisational turbulence’ which can critically undermine a group’s ability to maintain a safe yet challenging ‘formative space’. Academics at the University of Oxford studied the inter-organisational dynamics of a national democratic therapeutic community over a period of four years; they found external steering by authorities eroded the community’s therapeutic model, produced a crisis, and led to an intractable conflict which resulted in the community’s closure.

A form of group therapy has been reported to be effective in psychotic adolescents and recovering addicts. Projective psychotherapy uses an outside text such as a novel or motion picture to provide a “stable delusion” for the former cohort and a safe focus for repressed and suppressed emotions or thoughts in the latter. Patient groups read a novel or collectively view a film. They then participate collectively in the discussion of plot, character motivation and author motivation. In the case of films, sound track, cinematography and background are also discussed and processed. Under the guidance of the therapist, defence mechanisms are bypassed by the use of signifiers and semiotic processes. The focus remains on the text rather than on personal issues. It was popularised in the science fiction novel, Red Orc’s Rage.

Group therapy is now often utilised in private practice settings.

Group analysis has become widespread in Europe, and especially the United Kingdom, where it has become the most common form of group psychotherapy. Interest from Australia, the former Soviet Union and the African continent is also growing.

Research on Effectiveness

A 2008 meta-analysis found that individual therapy may be slightly more effective than group therapy initially, but this difference seems to disappears after 6 months. There is clear evidence for the effectiveness of group psychotherapy for depression: a meta-analysis of 48 studies showed an overall effect size of 1.03, which is clinically highly significant. Similarly, a meta-analysis of five studies of group psychotherapy for adult sexual abuse survivors showed moderate to strong effect sizes, and there is also good evidence for effectiveness with chronic traumatic stress in war veterans.

There is less robust evidence of good outcomes for patients with borderline personality disorder, with some studies showing only small to moderate effect sizes. The authors comment that these poor outcomes might reflect a need for additional support for some patients, in addition to the group therapy. This is borne out by the impressive results obtained using mentalisation-based treatment, a model that combines dynamic group psychotherapy with individual psychotherapy and case management.

Most outcome research is carried out using time-limited therapy with diagnostically homogenous groups. However, long-term intensive interactional group psychotherapy assumes diverse and diagnostically heterogeneous group membership, and an open-ended time scale for therapy. Good outcomes have also been demonstrated for this form of group therapy.

Computer-Supported Group Therapy

Research on computer-supported and computer-based interventions has increased significantly since the mid-1990s. For a comprehensive overview of current practices (refer to Computer-supported psychotherapy).

Several feasibility studies examined the impact of computer-, app- and media-support on group interventions. Most investigated interventions implemented short rationales, which usually were based on principles of cognitive behaviour therapy (CBT). Most research focussed on:

  • Anxiety disorders (e.g. social phobia, generalised anxiety disorder).
  • Depression (e.g. mild to moderate Major Depression).
  • Other disorders (e.g. hoarding).

While the evidence base for group therapy is very limited, preliminary research in individual therapy suggests possible increases of treatment efficiency or effectiveness. Further, the use of app- or computer-based monitoring has been investigated several times. Reported advantages of the modern format include improved between-session transfer and patient-therapist-communication, as well as increased treatment transparency and intensity. Negative effects may occur in terms of dissonance due to non-compliance with online tasks, or the constriction of in-session group interaction. Last but not least, group phenomena might influence the motivation to engage with online tasks.

What is Dispossession, Oppression, and Depression?

Introduction

Supplementing the medical model of depression, many researchers have begun to conceptualise ways in which the historical legacies of racism and colonialism create depressive conditions. Given the lived experiences of marginalised peoples, ranging from conditions of migration, class stratification, cultural genocide, labour exploitation, and social immobility, depression can be seen as a “rational response to global conditions”, according to Ann Cvetkovich.

Background

Psychogeographical depression overlaps somewhat with the theory of “deprejudice”, a portmanteau of depression and prejudice proposed by Cox, Abramson, Devine, and Hollon in 2012, who argue for an integrative approach to studying the often comorbid experiences. Cox, Abramson, Devine, and Hollon are concerned with the ways in which social stereotypes are often internalised, creating negative self-stereotypes that then produce depressive symptoms.

Unlike the theory of “deprejudice”, a psychogeographical theory of depression attempts to broaden study of the subject beyond an individual experience to one produced on a societal scale, seeing particular manifestations of depression as rooted in dispossession; historical legacies of genocide, slavery, and colonialism are productive of segregation, both material and psychic material deprivation, and concomitant circumstances of violence, systemic exclusion, and lack of access to legal protections. The demands of navigating these circumstances compromise the resources available to a population to seek comfort, health, stability, and sense of security. The historical memory of this trauma conditions the psychological health of future generations, making psychogeographical depression an intergenerational experience as well.

This work is supported by recent studies in genetic science which has demonstrated an epigenetic link between the trauma suffered by Holocaust survivors and the genetic reverberations for subsequent generations. Likewise, research by scientists at Emory University suggests that memories of trauma can be inherited, rendering offspring vulnerable to psychological predispositions for stress disorders, schizophrenia, and PTSD.

Vacant Lot Greening and Mood

A 2018 study asked low income residents of Philadelphia “how often they felt nervous, hopeless, restless, depressed and worthless.” As an experimental mental health intervention, trash was removed from vacant lots. Some of the vacant lots were “greened”, with plantings of trees, grass, and small fences. Residents near the “greened” lots who had incomes below the poverty line reported a decrease in feelings of depression of 68%, while residents with incomes above the poverty line reported a decrease of 41%. Removing trash from vacant lots without installing landscaping did not have an observable mental health impact.

What is Mood Disorder?

Introduction

Mood disorder, also known as mood affective disorders, is a group of conditions where a disturbance in the person’s mood is the main underlying feature. The classification is in the Diagnostic and Statistical Manual of Mental Disorders (DSM) and International Classification of Diseases (ICD).

Mood disorders fall into the basic groups of elevated mood, such as mania or hypomania; depressed mood, of which the best-known and most researched is major depressive disorder (MDD) (commonly called clinical depression, unipolar depression, or major depression); and moods which cycle between mania and depression, known as bipolar disorder (BD) (formerly known as manic depression). There are several sub-types of depressive disorders or psychiatric syndromes featuring less severe symptoms such as dysthymic disorder (similar to but milder than MDD) and cyclothymic disorder (similar to but milder than BD). Mood disorders may also be substance induced or occur in response to a medical condition.

English psychiatrist Henry Maudsley proposed an overarching category of affective disorder. The term was then replaced by mood-disorder, as the latter term refers to the underlying or longitudinal emotional state, whereas the former refers to the external expression observed by others.

Refer to Depression (Mood).

Epidemiology

According to a substantial amount of epidemiology studies conducted, women are twice as likely to develop certain mood disorders, such as major depression. Although there is an equal number of men and women diagnosed with bipolar II disorder, women have a slightly higher frequency of the disorder.

The prevalence of depressive symptoms has increased over the years with recent generations reporting a 6% increase in symptoms of depression compared to individuals from older generations.

In 2011, mood disorders were the most common reason for hospitalization among children aged 1-17 years in the United States, with approximately 112,000 stays. Mood disorders were top principal diagnosis for Medicaid super-utilisers in the United States in 2012. Further, a study of 18 States found that mood disorders accounted for the highest number of hospital readmissions among Medicaid patients and the uninsured, with 41,600 Medicaid patients and 12,200 uninsured patients being readmitted within 30 days of their index stay – a readmission rate of 19.8 per 100 admissions and 12.7 per 100 admissions, respectively. In 2012, mood and other behavioural health disorders were the most common diagnoses for Medicaid-covered and uninsured hospital stays in the United States (6.1% of Medicaid stays and 5.2% of uninsured stays).

A study conducted in 1988 to 1994 amongst young American adults involved a selection of demographic and health characteristics. A population-based sample of 8,602 men and women ages 17-39 years participated. Lifetime prevalence were estimated based on six mood measures:

  • Major depressive episode (MDE) 8.6%.
  • Major depressive disorder with severity (MDE-s) 7.7%.
  • Dysthymia 6.2%.
  • MDE-s with dysthymia 3.4%.
  • Any bipolar disorder 1.6%.
  • Any mood disorder 11.5%.

Classification

Depressive Disorders

  • Major depressive disorder (MDD):
    • Commonly called major depression, unipolar depression, or clinical depression, wherein a person has one or more major depressive episodes.
    • After a single episode, Major Depressive Disorder (single episode) would be diagnosed.
    • After more than one episode, the diagnosis becomes Major Depressive Disorder (Recurrent).
    • Depression without periods of mania is sometimes referred to as unipolar depression because the mood remains at the bottom “pole” and does not climb to the higher, manic “pole” as in bipolar disorder.
  • Individuals with a major depressive episode or major depressive disorder are at increased risk for suicide.
  • Seeking help and treatment from a health professional dramatically reduces the individual’s risk for suicide.
  • Studies have demonstrated that asking if a depressed friend or family member has thought of committing suicide is an effective way of identifying those at risk, and it does not “plant” the idea or increase an individual’s risk for suicide in any way.
  • Epidemiological studies carried out in Europe suggest that, at this moment, roughly 8.5% of the world’s population have a depressive disorder. No age group seems to be exempt from depression, and studies have found that depression appears in infants as young as 6 months old who have been separated from their mothers.
  • Depressive disorder is frequent in primary care and general hospital practice but is often undetected.
  • Unrecognised depressive disorder may slow recovery and worsen prognosis in physical illness, therefore it is important that all doctors be able to recognise the condition, treat the less severe cases, and identify those requiring specialist care.

Diagnosticians recognise several subtypes or course specifiers:

  • Atypical depression (AD):
    • This is characterised by mood reactivity (paradoxical anhedonia) and positivity, significant weight gain or increased appetite (“comfort eating”), excessive sleep or somnolence (hypersomnia), a sensation of heaviness in limbs known as leaden paralysis, and significant social impairment as a consequence of hypersensitivity to perceived interpersonal rejection.
    • Difficulties in measuring this subtype have led to questions of its validity and prevalence.
  • Melancholic depression:
    • This is characterised by a loss of pleasure (anhedonia) in most or all activities, a failure of reactivity to pleasurable stimuli, a quality of depressed mood more pronounced than that of grief or loss, a worsening of symptoms in the morning hours, early-morning waking, psychomotor retardation, excessive weight loss (not to be confused with anorexia nervosa), or excessive guilt.
  • Psychotic major depression (PMD):
    • Or simply psychotic depression, is the term for a major depressive episode, in particular of melancholic nature, wherein the patient experiences psychotic symptoms such as delusions or, less commonly, hallucinations.
    • These are most commonly mood-congruent (content coincident with depressive themes).
  • Catatonic depression:
    • This is a rare and severe form of major depression involving disturbances of motor behaviour and other symptoms.
    • Here, the person is mute and almost stuporose, and either is immobile or exhibits purposeless or even bizarre movements.
    • Catatonic symptoms can also occur in schizophrenia or a manic episode, or can be due to neuroleptic malignant syndrome.
  • Postpartum depression (PPD)
    • This is listed as a course specifier in DSM-IV-TR; it refers to the intense, sustained and sometimes disabling depression experienced by women after giving birth.
    • Postpartum depression, which affects 10-15% of women, typically sets in within three months of labour, and lasts as long as three months.
    • It is quite common for women to experience a short-term feeling of tiredness and sadness in the first few weeks after giving birth; however, postpartum depression is different because it can cause significant hardship and impaired functioning at home, work, or school as well as, possibly, difficulty in relationships with family members, spouses, or friends, or even problems bonding with the newborn.
    • In the treatment of postpartum major depressive disorders and other unipolar depressions in women who are breastfeeding, nortriptyline, paroxetine (Paxil), and sertraline (Zoloft) are in general considered to be the preferred medications.
    • Women with personal or family histories of mood disorders are at particularly high risk of developing postpartum depression.
  • Premenstrual dysphoric disorder (PMDD):
    • This is a severe and disabling form of premenstrual syndrome affecting 3-8% of menstruating women.
    • The disorder consists of a “cluster of affective, behavioural and somatic symptoms” that recur monthly during the luteal phase of the menstrual cycle.
    • PMDD was added to the list of depressive disorders in the Diagnostic and Statistical Manual of Mental Disorders in 2013.
    • The exact pathogenesis of the disorder is still unclear and is an active research topic. Treatment of PMDD relies largely on antidepressants that modulate serotonin levels in the brain via serotonin reuptake inhibitors as well as ovulation suppression using contraception.
  • Seasonal affective disorder (SAD):
    • Also known as “winter depression” or “winter blues”, is a specifier.
    • Some people have a seasonal pattern, with depressive episodes coming on in the autumn or winter, and resolving in spring.
    • The diagnosis is made if at least two episodes have occurred in colder months with none at other times over a two-year period or longer.
    • It is commonly hypothesised that people who live at higher latitudes tend to have less sunlight exposure in the winter and therefore experience higher rates of SAD, but the epidemiological support for this proposition is not strong (and latitude is not the only determinant of the amount of sunlight reaching the eyes in winter).
    • It is said that this disorder can be treated by light therapy.
    • SAD is also more prevalent in people who are younger and typically affects more females than males.
  • Dysthymia:
    • This is a condition related to unipolar depression, where the same physical and cognitive problems are evident, but they are not as severe and tend to last longer (usually at least 2 years).
    • The treatment of dysthymia is largely the same as for major depression, including antidepressant medications and psychotherapy.
  • Double depression:
    • Can be defined as a fairly depressed mood (dysthymia) that lasts for at least two years and is punctuated by periods of major depression.
  • Depressive Disorder Not Otherwise Specified (DD-NOS):
    • This is designated by the code 311 for depressive disorders that are impairing but do not fit any of the officially specified diagnoses.
    • According to the DSM-IV, DD-NOS encompasses “any depressive disorder that does not meet the criteria for a specific disorder.”
    • It includes the research diagnoses of recurrent brief depression, and minor depressive disorder listed below.
  • Depressive personality disorder (DPD)
    • This is a controversial psychiatric diagnosis that denotes a personality disorder with depressive features.
    • Originally included in the DSM-II, depressive personality disorder was removed from the DSM-III and DSM-III-R.
    • Recently, it has been reconsidered for reinstatement as a diagnosis. Depressive personality disorder is currently described in Appendix B in the DSM-IV-TR as worthy of further study.
  • Recurrent brief depression (RBD):
    • Distinguished from major depressive disorder primarily by differences in duration.
    • Individuals with RBD have depressive episodes about once per month, with individual episodes lasting less than two weeks and typically less than 2-3 days.
    • Diagnosis of RBD requires that the episodes occur over the span of at least one year and, in female patients, independently of the menstrual cycle.
    • Individuals with clinical depression can develop RBD, and vice versa, and both illnesses have similar risks.
  • Minor depressive disorder:
    • Or simply minor depression, which refers to a depression that does not meet full criteria for major depression but in which at least two symptoms are present for two weeks.

Bipolar Disorders

Bipolar disorder (BD) (also called “manic depression” or “manic-depressive disorder”), an unstable emotional condition characterised by cycles of abnormal, persistent high mood (mania) and low mood (depression), which was formerly known as “manic depression” (and in some cases rapid cycling, mixed states, and psychotic symptoms). Subtypes include:

  • Bipolar I:
    • This is distinguished by the presence or history of one or more manic episodes or mixed episodes with or without major depressive episodes.
    • A depressive episode is not required for the diagnosis of Bipolar I Disorder, but depressive episodes are usually part of the course of the illness.
  • Bipolar II :
    • Consisting of recurrent intermittent hypomanic and depressive episodes or mixed episodes.
  • Cyclothymia:
    • This is a form of bipolar disorder, consisting of recurrent hypomanic and dysthymic episodes, but no full manic episodes or full major depressive episodes.
  • Bipolar disorder not otherwise specified (BD-NOS):
    • Sometimes called “sub-threshold” bipolar, indicates that the patient has some symptoms in the bipolar spectrum (e.g. manic and depressive symptoms) but does not fully qualify for any of the three formal bipolar DSM-IV diagnoses mentioned above.

It is estimated that roughly 1% of the adult population has bipolar I, a further 1% has bipolar II or cyclothymia, and somewhere between 2% and 5% percent have “sub-threshold” forms of bipolar disorder. Furthermore, the possibility of getting bipolar disorder when one parent is diagnosed with it is 15-30%. Risk, when both parents have it, is 50-75%. Also, while with bipolar siblings the risk is 15-25%, with identical twins it is about 70%.

A minority of people with bipolar disorder have high creativity, artistry or a particular gifted talent. Before the mania phase becomes too extreme, its energy, ambition, enthusiasm and grandiosity often bring people with this type of mood disorder life’s masterpieces.[29]

Substance-induced

A mood disorder can be classified as substance-induced if its aetiology can be traced to the direct physiologic effects of a psychoactive drug or other chemical substance, or if the development of the mood disorder occurred contemporaneously with substance intoxication or withdrawal. Also, an individual may have a mood disorder coexisting with a substance abuse disorder. Substance-induced mood disorders can have features of a manic, hypomanic, mixed, or depressive episode. Most substances can induce a variety of mood disorders. For example, stimulants such as amphetamine, methamphetamine, and cocaine can cause manic, hypomanic, mixed, and depressive episodes.

Alcohol-Induced

High rates of major depressive disorder occur in heavy drinkers and those with alcoholism. Controversy has previously surrounded whether those who abused alcohol and developed depression were self-medicating their pre-existing depression. But recent research has concluded that, while this may be true in some cases, alcohol misuse directly causes the development of depression in a significant number of heavy drinkers. Participants studied were also assessed during stressful events in their lives and measured on a Feeling Bad Scale. Likewise, they were also assessed on their affiliation with deviant peers, unemployment, and their partner’s substance use and criminal offending. High rates of suicide also occur in those who have alcohol-related problems. It is usually possible to differentiate between alcohol-related depression and depression that is not related to alcohol intake by taking a careful history of the patient. Depression and other mental health problems associated with alcohol misuse may be due to distortion of brain chemistry, as they tend to improve on their own after a period of abstinence.

Benzodiazepine-induced

Benzodiazepines, such as alprazolam, clonazepam, lorazepam and diazepam, can cause both depression and mania.

Benzodiazepines are a class of medication commonly used to treat anxiety, panic attacks and insomnia, and are also commonly misused and abused. Those with anxiety, panic and sleep problems commonly have negative emotions and thoughts, depression, suicidal ideations, and often have comorbid depressive disorders. While the anxiolytic and hypnotic effects of benzodiazepines disappear as tolerance develops, depression and impulsivity with high suicidal risk commonly persist. These symptoms are “often interpreted as an exacerbation or as a natural evolution of previous disorders and the chronic use of sedatives is overlooked”. Benzodiazepines do not prevent the development of depression, can exacerbate pre-existing depression, can cause depression in those with no history of it, and can lead to suicide attempts. Risk factors for attempted and completed suicide while using benzodiazepines include high dose prescriptions (even in those not misusing the medications), benzodiazepine intoxication, and underlying depression.

The long-term use of benzodiazepines may have a similar effect on the brain as alcohol, and are also implicated in depression. As with alcohol, the effects of benzodiazepine on neurochemistry, such as decreased levels of serotonin and norepinephrine, are believed to be responsible for the increased depression. Additionally, benzodiazepines can indirectly worsen mood by worsening sleep (i.e. benzodiazepine-induced sleep disorder). Like alcohol, benzodiazepines can put people to sleep but, while asleep, they disrupt sleep architecture: decreasing sleep time, delaying time to REM sleep, and decreasing deep sleep (the most restorative part of sleep for both energy and mood). Just as some antidepressants can cause or worsen anxiety in some patients due to being activating, benzodiazepines can cause or worsen depression due to being a central nervous system depressant – worsening thinking, concentration and problem solving (i.e. benzodiazepine-induced neurocognitive disorder). However, unlike antidepressants, in which the activating effects usually improve with continued treatment, benzodiazepine-induced depression is unlikely to improve until after stopping the medication.

In a long-term follow-up study of patients dependent on benzodiazepines, it was found that 10 people (20%) had taken drug overdoses while on chronic benzodiazepine medication despite only two people ever having had any pre-existing depressive disorder. A year after a gradual withdrawal programme, no patients had taken any further overdoses.

Just as with intoxication and chronic use, benzodiazepine withdrawal can also cause depression. While benzodiazepine-induced depressive disorder may be exacerbated immediately after discontinuation of benzodiazepines, evidence suggests that mood significantly improves after the acute withdrawal period to levels better than during use. Depression resulting from withdrawal from benzodiazepines usually subsides after a few months but in some cases may persist for 6-12 months.

Due to Another Medical Condition

“Mood disorder due to a general medical condition” is used to describe manic or depressive episodes which occur secondary to a medical condition. There are many medical conditions that can trigger mood episodes, including neurological disorders (e.g. dementias), metabolic disorders (e.g. electrolyte disturbances), gastrointestinal diseases (e.g. cirrhosis), endocrine disease (e.g. thyroid abnormalities), cardiovascular disease (e.g. heart attack), pulmonary disease (e.g. chronic obstructive pulmonary disease), cancer, and autoimmune diseases (e.g. multiple sclerosis).

Not Otherwise Specified

Mood disorder not otherwise specified (MD-NOS) is a mood disorder that is impairing but does not fit in with any of the other officially specified diagnoses. In the DSM-IV MD-NOS is described as “any mood disorder that does not meet the criteria for a specific disorder.” MD-NOS is not used as a clinical description but as a statistical concept for filing purposes.

Most cases of MD-NOS represent hybrids between mood and anxiety disorders, such as mixed anxiety-depressive disorder or atypical depression. An example of an instance of MD-NOS is being in minor depression frequently during various intervals, such as once every month or once in three days. There is a risk for MD-NOS not to get noticed, and for that reason not to get treated.

Causes

Meta-analyses show that high scores on the personality domain neuroticism are a strong predictor for the development of mood disorders. A number of authors have also suggested that mood disorders are an evolutionary adaptation. A low or depressed mood can increase an individual’s ability to cope with situations in which the effort to pursue a major goal could result in danger, loss, or wasted effort. In such situations, low motivation may give an advantage by inhibiting certain actions. This theory helps to explain why negative life incidents precede depression in around 80% of cases, and why they so often strike people during their peak reproductive years. These characteristics would be difficult to understand if depression were a dysfunction.

A depressed mood is a predictable response to certain types of life occurrences, such as loss of status, divorce, or death of a child or spouse. These are events that signal a loss of reproductive ability or potential, or that did so in humans’ ancestral environment. A depressed mood can be seen as an adaptive response, in the sense that it causes an individual to turn away from the earlier (and reproductively unsuccessful) modes of behaviour.

A depressed mood is common during illnesses, such as influenza. It has been argued that this is an evolved mechanism that assists the individual in recovering by limiting his/her physical activity. The occurrence of low-level depression during the winter months, or seasonal affective disorder, may have been adaptive in the past, by limiting physical activity at times when food was scarce. It is argued that humans have retained the instinct to experience low mood during the winter months, even if the availability of food is no longer determined by the weather.

Much of what is known about the genetic influence of clinical depression is based upon research that has been done with identical twins. Identical twins have exactly the same genetic code. It has been found that when one identical twin becomes depressed the other will also develop clinical depression approximately 76% of the time. When identical twins are raised apart from each other, they will both become depressed about 67% of the time. Because both twins become depressed at such a high rate, the implication is that there is a strong genetic influence. If it happened that when one twin becomes clinically depressed the other always develops depression, then clinical depression would likely be entirely genetic.

Bipolar disorder is also considered a mood disorder and it is hypothesized that it might be caused by mitochondrial dysfunction.

Sex Differences

Mood disorders, specifically stress-related mood disorders such as anxiety and depression, have been shown to have differing rates of diagnosis based on sex. In the United States, women are two times more likely than men to be diagnosed with a stress-related mood disorder. Underlying these sex differences, studies have shown a dysregulation of stress-responsive neuroendocrine function causing an increase in the likelihood of developing these affective disorders. Overactivation of the hypothalamic-pituitary-adrenal (HPA) axis could provide potential insight into how these sex differences arise. Neuropeptide corticotropin-releasing factor (CRF) is released from the paraventricular nucleus (PVN) of the hypothalamus, stimulating adrenocorticotropic hormone (ACTH) release into the blood stream. From here ACTH triggers the release of glucocorticoids such as cortisol from the adrenal cortex. Cortisol, known as the main stress hormone, creates a negative feedback loop back to the hypothalamus to deactivate the stress response. When a constant stressor is present, the HPA axis remains overactivated and cortisol is constantly produced. This chronic stress is associated with sustained CRF release, resulting in the increased production of anxiety- and depressive-like behaviours and serving as a potential mechanism for differences in prevalence between men and women.

Diagnosis

DSM-5

The DSM-5, released in May 2013, separates the mood disorder chapter from the DSM-TR-IV into two sections: Depressive and related disorders and bipolar and related disorders. Bipolar disorders falls in between depressive disorders and schizophrenia spectrum and related disorders “in recognition of their place as a bridge between the two diagnostic classes in terms of symptomatology, family history and genetics” (Ref. 1, p 123). Bipolar disorders underwent a few changes in the DSM-5, most notably the addition of more specific symptomology related to hypomanic and mixed manic states. Depressive disorders underwent the most changes, the addition of three new disorders: disruptive mood dysregulation disorder, persistent depressive disorder (previously dysthymia), and premenstrual dysphoric disorder (previously in appendix B, the section for disorders needing further research). Disruptive mood dysregulation disorder is meant as a diagnosis for children and adolescents who would normally be diagnosed with bipolar disorder as a way to limit the bipolar diagnosis in this age cohort. Major depressive disorder (MDD) also underwent a notable change, in that the bereavement clause has been removed. Those previously exempt from a diagnosis of MDD due to bereavement are now candidates for the MDD diagnosis.

Treatment

There are different types of treatments available for mood disorders, such as therapy and medications. Behaviour therapy, cognitive behaviour therapy and interpersonal therapy have all shown to be potentially beneficial in depression. Major depressive disorder medications usually include antidepressants; a combination of antidepressants and cognitive behavioural therapy has shown to be more effective than one treatment alone. Bipolar disorder medications can consist of antipsychotics, mood stabilisers, anticonvulsants and/or lithium. Lithium specifically has been proven to reduce suicide and all causes of mortality in people with mood disorders. If mitochondrial dysfunction or mitochondrial diseases are the cause of mood disorders like bipolar disorder, then it has been hypothesized that N-acetyl-cysteine (NAC), acetyl-L-carnitine (ALCAR), S-adenosylmethionine (SAMe), coenzyme Q10 (CoQ10), alpha-lipoic acid (ALA), creatine monohydrate (CM), and melatonin could be potential treatment options. In determining treatment, there are many types of depression scales that are used.

  • One of the depression scales is a self-report scale called Beck Depression Inventory (BDI).
  • Another scale is the Hamilton Depression Rating Scale (HAMD).
    • HAMD is a clinical rating scale in which the patient is rated based on clinician observation.
  • The Centre for Epidemiologic Studies Depression Scale (CES-D) is a scale for depression symptoms that applies to the general population.
    • This scale is typically used in research and not for self-reports.
  • The PHQ-9 which stands for Patient-Health Questionnaire-9 questions, is a self-report as well.
  • Finally, the Mood Disorder Questionnaire (MDQ) evaluates bipolar disorder.

Research

Kay Redfield Jamison and others have explored the possible links between mood disorders – especially bipolar disorder – and creativity. It has been proposed that a “ruminating personality type may contribute to both [mood disorders] and art.”

Jane Collingwood notes an Oregon State University study that:

“…looked at the occupational status of a large group of typical patients and found that ‘those with bipolar illness appear to be disproportionately concentrated in the most creative occupational category.’ They also found that the likelihood of ‘engaging in creative activities on the job’ is significantly higher for bipolar than nonbipolar workers”.

In Liz Paterek’s article “Bipolar Disorder and the Creative Mind” she wrote:

“Memory and creativity are related to mania. Clinical studies have shown that those in a manic state will rhyme, find synonyms, and use alliteration more than controls. This mental fluidity could contribute to an increase in creativity. Moreover, mania creates increases in productivity and energy. Those in a manic state are more emotionally sensitive and show less inhibition about attitudes, which could create greater expression. Studies performed at Harvard looked into the amount of original thinking in solving creative tasks. Bipolar individuals, whose disorder was not severe, tended to show greater degrees of creativity.”

The relationship between depression and creativity appears to be especially strong among poets.

What are the Differential Diagnoses of Depression?

Introduction

Depression, one of the most commonly diagnosed psychiatric disorders, is being diagnosed in increasing numbers in various segments of the population worldwide. For example, depression in the United States (US) alone affects 17.6 million Americans each year or 1 in 6 people. Depressed patients are at increased risk of type 2 diabetes, cardiovascular disease and suicide. Within the next twenty years depression is expected to become the second leading cause of disability worldwide and the leading cause in high-income nations, including the US. In approximately 75% of completed suicides, the individuals had seen a physician within the prior year before their death, 45-66% within the prior month. About a third of those who completed suicide had contact with mental health services in the prior year, a fifth within the preceding month.

There are many psychiatric and medical conditions that may mimic some or all of the symptoms of depression or may occur comorbid to it. A disorder either psychiatric or medical that shares symptoms and characteristics of another disorder, and may be the true cause of the presenting symptoms is known as a differential diagnosis.

Many psychiatric disorders such as depression are diagnosed by allied health professionals with little or no medical training, and are made on the basis of presenting symptoms without proper consideration of the underlying cause, adequate screening of differential diagnoses is often not conducted. According to one study, non-medical mental health care providers may be at increased risk of not recognising masked medical illnesses in their patients.

Misdiagnosis or missed diagnoses may lead to lack of treatment or ineffective and potentially harmful treatment which may worsen the underlying causative disorder. A conservative estimate is that 10% of all psychological symptoms may be due to medical reasons, with the results of one study suggesting that about half of individuals with a serious mental illness have general medical conditions that are largely undiagnosed and untreated and may cause or exacerbate psychiatric symptoms.

In a case of misdiagnosed depression recounted in Newsweek, a writer received treatment for depression for years; during the last 10 years of her depression the symptoms worsened, resulting in multiple suicide attempts and psychiatric hospitalisations. When an MRI finally was performed, it showed the presence of a tumour. However, she was told by a neurologist that it was benign. After a worsening of symptoms, and upon the second opinion of another neurologist, the tumour was removed. After the surgery, she no longer suffered from depressive symptoms.

Autoimmune Disorders

  • Celiac disease:
    • This is an autoimmune disorder in which the body is unable to digest gluten which is found in various food grains, most notably wheat, and also rye and barley.
    • Current research has shown its neuropsychiatric symptoms may manifest without the gastrointestinal symptoms.
    • However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology.
  • Lupus:
    • Systemic lupus erythematosus (SLE), is a chronic autoimmune connective tissue disease that can affect any part of the body.
    • Lupus can cause or worsen depression.

Bacterial-Viral-Parasitic Infection

  • Lyme disease:
    • This is a bacterial infection caused by Borrelia burgdorferi, a spirochete bacterium transmitted by the Deer tick (Ixodes scapularis).
    • Lyme disease is one of a group of diseases which have earned the name the “great imitator” for their propensity to mimic the symptoms of a wide variety of medical and neuropsychiatric disorders.
    • Lyme disease is an underdiagnosed illness, partially as a result of the complexity and unreliability of serologic testing.
    • Because of the rapid rise of Lyme borreliosis nationwide and the need for antibiotic treatment to prevent severe neurologic damage, mental health professionals need to be aware of its possible psychiatric presentations.
  • Syphilis:
    • The prevalence of which is on the rise, is another of the “great imitators”, which if left untreated can progress to neurosyphilis and affect the brain, can present with solely neuropsychiatric symptoms.
    • This case emphasises that neurosyphilis still has to be considered in the differential diagnosis within the context of psychiatric conditions and diseases.
    • Owing to current epidemiological data and difficulties in diagnosing syphilis, routine screening tests in the psychiatric field are necessary.
  • Neurocysticercosis (NCC):
    • This is an infection of the brain or spinal cord caused by the larval stage of the pork tapeworm, Taenia solium.
    • NCC is the most common helminthic (parasitic worm) infestation of the central nervous system worldwide. Humans develop cysticercosis when they ingest eggs of the pork tapeworm via contact with contaminated fecal matter or eating infected vegetables or undercooked pork.
    • While cysticercosis is endemic in Latin America, it is an emerging disease with increased prevalence in the United States.
    • The rate of depression in those with neurocysticercosis is higher than in the general population.
  • Toxoplasmosis:
    • This is an infection caused by Toxoplasma gondii an intracellular protozoan parasite. Humans can be infected in 3 different ways:
      • Ingestion of tissue cysts;
      • Ingestion of oocysts; or
      • In utero infection with tachyzoites.
    • One of the prime methods for transmission to humans is contact with the faeces of the host species, the domesticated cat.
    • Toxoplasma gondii infects approximately 30% of the world’s human population, but causes overt clinical symptoms in only a small segment of those infected.
    • Exposure to Toxoplasma gondii (seropositivity) without developing Toxoplasmosis has been proven to alter various characteristics of human behaviour as well as being a causative factor in some cases of depression, in addition, studies have linked seropositivity with an increased rate of suicide
  • West Nile virus (WNV):
    • This can cause encephalitis has been reported to be a causal factor in developing depression in 31% of those infected in a study conducted in Houston, Texas and reported to the Centre for Disease Control (CDC).
    • The primary vectors for disease transmission to humans are various species of mosquito.
    • WNV which is endemic to Southern Europe, Africa the Middle East and Asia was first identified in the United States in 1999.
    • Between 1999 and 2006, 20,000 cases of confirmed symptomatic WNV were reported in the US, with estimates of up to 1 million being infected.
    • WNV is now the most common cause of epidemic viral encephalitis in the United States, and it will likely remain an important cause of neurological disease for the foreseeable future.

Blood Disorders

  • Anaemia:
    • This is a decrease in normal number of red blood cells (RBCs) or less than the normal quantity of haemoglobin in the blood.
    • Depressive symptoms are associated with anaemia in a general population of older persons living in the community.

Chronic Fatigue Syndrome

Between 1 and 4 million Americans are believed to have chronic fatigue syndrome (CFS), yet only 50% have consulted a physician for symptoms of CFS. In addition individuals with CFS symptoms often have an undiagnosed medical or psychiatric disorder such as diabetes, thyroid disease or substance abuse. CFS, at one time considered to be psychosomatic in nature, is now considered to be a valid medical condition in which early diagnosis and treatment can aid in alleviating or completely resolving symptoms. While frequently misdiagnosed as depression, differences have been noted in rate of cerebral blood flow.

CFS is underdiagnosed in more than 80% of the people who have it; at the same time, it is often misdiagnosed as depression.

Dietary Disorders

  • Fructose malabsorption and lactose intolerance; deficient fructose transport by the duodenum, or by the deficiency of the enzyme, lactase in the mucosal lining, respectively.
  • As a result of this malabsorption the saccharides reach the colon and are digested by bacteria which convert them to short chain fatty acids, CO2, and H2.
  • Approximately 50% of those afflicted exhibit the physical signs of irritable bowel syndrome.
  • Fructose malabsorption may play a role in the development of depressed mood. Fructose malabsorption should be considered in patients with symptoms of major depression.
  • Fructose and sorbitol reduced diet in subjects with fructose malabsorption does not only reduce gastrointestinal symptoms but also improves mood and early signs of depression.

Endocrine System Disorders

Dysregulation of the endocrine system may present with various neuropsychiatric symptoms; irregularities in the hypothalamic-pituitary- adrenal (HPA) axis and the hypothalamic-pituitary-thyroid (HPT) axis have been shown in patients with primary depression.

HPT and HPA axes abnormalities observed in patients with depression:

  • HPT axes irregularities:
    • Alterations in thyroid-stimulating hormone (TSH) response to thyrotropin-releasing hormone (TRH).
    • An abnormally high rate of antithyroid antibodies.
    • Elevated cerebrospinal fluid (CSF) TRH concentrations.
  • HPA axes irregularities:
    • Adrenocorticoid hypersecretion.
    • Enlarged pituitary and adrenal gland size (organomegaly).
    • Elevated corticotropin-releasing factor (CSF) concentrations.

Adrenal Gland

  • Addison’s disease:
    • Also known as chronic adrenal insufficiency, hypocortisolism, and hypocorticism) is a rare endocrine disorder wherein the adrenal glands, located above the kidneys, produce insufficient steroid hormones (glucocorticoids and often mineralocorticoids).
    • Addison’s disease presenting with psychiatric features in the early stage has the tendency to be overlooked and misdiagnosed.
  • Cushing’s Syndrome:
    • Also known as hypercortisolism, is an endocrine disorder characterised by an excess of cortisol.
    • In the absence of prescribed steroid medications, it is caused by a tumour on the pituitary or adrenal glands, or more rarely, an ectopic hormone-secreting tumour.
    • Depression is a common feature in diagnosed patients and it often improves with treatment.

Thyroid and Parathyroid Glands

  • Graves’ disease:
    • An autoimmune disease where the thyroid is overactive, resulting in hyperthyroidism and thyrotoxicosis.
  • Hashimoto’s thyroiditis:
    • Also known chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed by a variety of cell and antibody mediated immune processes.
    • Hashimoto’s thyroiditis is associated with thyroid peroxidase and thyroglobulin autoantibodies
  • Hashitoxicosis.
  • Hypothyroidism.
  • Hyperthyroidism.
  • Hypoparathyroidism:
    • Can affect calcium homeostasis, supplementation of which has completely resolved cases of depression in which hypoparathyroidism is the sole causative factor.

Pituitary Tumours

Tumours of the pituitary gland are fairly common in the general population with estimates ranging as high as 25%. Most tumours are considered to be benign and are often an incidental finding discovered during autopsy or as of neuroimaging in which case they are dubbed “incidentalomas”. Even in benign cases, pituitary tumours can affect cognitive, behavioural and emotional changes. Pituitary microadenomas are smaller than 10 mm in diameter and are generally considered benign, yet the presence of a microadenoma has been positively identified as a risk factor for suicide.

Patients with pituitary disease are diagnosed and treated for depression and show little response to the treatment for depression.

Pancreas

  • Hypoglycemia:
    • An overproduction of insulin causes reduced blood levels of glucose.
    • In one study of patients recovering from acute lung injury in intensive care, those patients who developed hypoglycaemia while hospitalised showed an increased rate of depression.

Neurological

Central Nervous System Tumours

In addition to pituitary tumours, tumours in various locations in the central nervous system (CNS) may cause depressive symptoms and be misdiagnosed as depression.

Post Concussion Syndrome

Post-concussion syndrome (PCS), is a set of symptoms that a person may experience for weeks, months, or occasionally years after a concussion with a prevalence rate of 38-80% in mild traumatic brain injuries, it may also occur in moderate and severe cases of traumatic brain injury. A diagnosis may be made when symptoms resulting from concussion, depending on criteria, last for more than three to six months after the injury, in which case it is termed persistent post-concussive syndrome (PPCS). In a study of the prevalence of post concussion syndrome symptoms in patients with depression utilising the British Columbia Post-concussion Symptom Inventory: “Approximately 9 out of 10 patients with depression met liberal self-report criteria for a post-concussion syndrome and more than 5 out of 10 met conservative criteria for the diagnosis.” These self reported rates were significantly higher than those obtained in a scheduled clinical interview. Normal controls have exhibited symptoms of PCS as well as those seeking psychological services. There is considerable debate over the diagnosis of PCS in part because of the medico-legal and thus monetary ramifications of receiving the diagnosis.

Pseudobulbar Affect

Pseudobulbar affect (PBA) is an affective disinhibition syndrome that is largely unrecognised in clinical settings and thus often untreated due to ignorance of the clinical manifestations of the disorder; it may be misdiagnosed as depression. It often occurs secondary to various neurodegenerative diseases such as amyotrophic lateral sclerosis, and also can result from head trauma. PBA is characterised by involuntary and inappropriate outbursts of laughter and/or crying. PBA has a high prevalence rate with estimates of 1.5-2 million cases in the United States alone.

Multiple Sclerosis

Multiple sclerosis is a chronic demyelinating disease in which the myelin sheaths of cells in the brain and spinal cord are irreparably damaged. Symptoms of depression are very common in patients at all stages of the disease and may be exacerbated by medical treatments, notably interferon beta-1a.

Neurotoxicity

Various compounds have been shown to have neurotoxic effects many of which have been implicated as having a causal relationship in the development of depression.

Cigarette Smoking

There has been research which suggests a correlation between cigarette smoking and depression. The results of one recent study suggest that smoking cigarettes may have a direct causal effect on the development of depression. There have been various studies done showing a positive link between smoking, suicidal ideation and suicide attempts.

In a study conducted among nurses, those smoking between 1-24 cigarettes per day had twice the suicide risk; 25 cigarettes or more, 4 times the suicide risk, than those who had never smoked. In a study of 300,000 male US Army soldiers, a definitive link between suicide and smoking was observed with those smoking over a pack a day having twice the suicide rate of non-smokers.

Medication

Various medications have been suspected of having a causal relation in the development of depression; this has been classified as “organic mood syndrome”. Some classes of medication such as those used to treat hypertension, have been recognised for decades as having a definitive relationship with the development of depression.

Monitoring of those taking medications which have shown a relationship with depression is often indicated, as well as the necessity of factoring in the use of such medications in the diagnostic process.

  • Topical Tretinoin (Retin-A):
    • Derived from Vitamin A and used for various medical conditions such as in topical solutions used to treat acne vulgaris.
    • Although applied externally to the skin, it may enter the bloodstream and cross the blood brain barrier where it may have neurotoxic effects.
  • Interferons:
    • Proteins produced by the human body, three types have been identified alpha, beta and gamma.
    • Synthetic versions are utilised in various medications used to treat different medical conditions such as the use of interferon-alpha in cancer treatment and hepatitis C treatment.
    • All three classes of interferons may cause depression and suicidal ideation.

Chronic Exposure to Organophosphates

The neuropsychiatric effects of chronic organophosphate exposure include mood disorders, suicidal thinking and behaviour, cognitive impairment and chronic fatigue.

Neuropsychiatric

Bipolar Disorder

Bipolar disorder is frequently misdiagnosed as major depression, and is thus treated with antidepressants alone which is not only not efficacious it is often contraindicated as it may exacerbate hypomania, mania, or cycling between moods. There is ongoing debate about whether this should be classified as a separate disorder because individuals diagnosed with major depression often experience some hypomanic symptoms, indicating a continuum between the two.

Nutritional Deficiencies

Nutrition plays a key role in every facet of maintaining proper physical and psychological wellbeing. Insufficient or inadequate nutrition can have a profound effect on mental health. The emerging field of nutritional neuroscience explores the various connections between diet, neurological functioning and mental health.

  • Vitamin B6:
    • Pyridoxal phosphate (PLP), the active form of B6, is a cofactor in the dopamine serotonin pathway, a deficiency in vitamin B6 may cause depressive symptoms.
  • Folate (vitamin B9) – Vitamin B12 cobalamin:
    • Low blood plasma and particularly red cell folate and diminished levels of vitamin B12 have been found in patients with depressive disorders.
    • Research suggests that oral doses of both folic acid (800 μg/(mcg) daily) and vitamin B12 (1 mg daily) should be tried to improve treatment outcome in depression.
  • Long chain fatty acids:
    • Higher levels of omega-6 and lower levels of omega-3 fatty acids has been associated with depression and behavioural change.
  • Vitamin D deficiency is associated with depression

Sleep Disorders

  • Insomnia:
    • While the inability to fall asleep is often a symptom of depression, it can also in some instances serve as the trigger for developing a depressive disorder.
    • It can be transient, acute or chronic.
    • It can be a primary disorder or a co-morbid one.
  • Restless legs syndrome (RLS):
    • Also known as Wittmaack-Ekbom’s syndrome, is characterised by an irresistible urge to move one’s body to stop uncomfortable or odd sensations.
    • It most commonly affects the legs, but can also affect the arms or torso, and even phantom limbs.
    • Restless Leg syndrome has been associated with Major depressive disorder.
    • Adjusted odds ratio for diagnosis of major depressive disorder suggest a strong association between restless legs syndrome and major depressive disorder and/or panic disorder.
  • Sleep apnea:
    • This is a sleep disorder characterised by pauses in breathing during sleep.
    • Each episode, called an apnoea, lasts long enough for one or more breaths to be missed; such episodes occur repeatedly throughout the sleep cycle.
    • Undiagnosed sleep apnoea may cause or contribute to the severity of depression.
  • Circadian rhythm sleep disorders:
    • Few clinicians are aware, and often goes untreated or are treated inappropriately, as when misdiagnosed as either primary insomnia or as a psychiatric condition.

What is Depression (Mood)?

Introduction

Depression is a state of low mood and aversion to activity. It can affect a person’s thoughts, behaviour, motivation, feelings, and sense of well-being.

The core symptom of depression is said to be anhedonia, which refers to loss of interest or a loss of feeling of pleasure in certain activities that usually bring joy to people. Depressed mood is a symptom of some mood disorders such as major depressive disorder or dysthymia; it is a normal temporary reaction to life events, such as the loss of a loved one; and it is also a symptom of some physical diseases and a side effect of some drugs and medical treatments.

It may feature sadness, difficulty in thinking and concentration and a significant increase or decrease in appetite and time spent sleeping. People experiencing depression may have feelings of dejection, hopelessness and, sometimes, suicidal thoughts. It can either be short term or long term.

Epidemiology

Depression is the leading cause of disability worldwide, the United Nations (UN) health agency reported, estimating that it affects more than 300 million people worldwide – the majority of them women, young people and the elderly. An estimated 4.4% of the global population suffers from depression, according to a report released by the UN World Health Organisation (WHO), which shows an 18 percent increase in the number of people living with depression between 2005 and 2015.

Global Health

Depression is a major mental-health cause of disease burden. Its consequences further lead to significant burden in public health, including a higher risk of dementia, premature mortality arising from physical disorders, and maternal depression impacts on child growth and development. Approximately 76% to 85% of depressed people in low- and middle-income countries do not receive treatment;[48] barriers to treatment include: inaccurate assessment, lack of trained health-care providers, social stigma and lack of resources.

The WHO has constructed guidelines – known as The Mental Health Gap Action Programme (mhGAP) – aiming to increase services for people with mental, neurological and substance-use disorders. Depression is listed as one of conditions prioritised by the programme. Trials conducted show possibilities for the implementation of the programme in low-resource primary-care settings dependent on primary-care practitioners and lay health-workers. Examples of mhGAP-endorsed therapies targeting depression include Group Interpersonal Therapy as group treatment for depression and “Thinking Health”, which utilises cognitive behavioural therapy to tackle perinatal depression. Furthermore, effective screening in primary care is crucial for the access of treatments. The mhGAP programme adopted its approach of improving detection rates of depression by training general practitioners. However, there is still weak evidence supporting this training.

History of the Concept

The Greco-Roman world used the tradition of the four humours to attempt to systematise sadness as “melancholia”.

The well-established idea of melancholy fell out of scientific favour in the 19th century.

Emil Kraepelin tried to give a scientific account of depression (German: das manisch-depressive Irresein) in 1896.

Factors

Life Events

Adversity in childhood, such as bereavement, neglect, mental abuse, physical abuse, sexual abuse, or unequal parental treatment of siblings can contribute to depression in adulthood. Childhood physical or sexual abuse in particular significantly correlates with the likelihood of experiencing depression over the victim’s lifetime.

Life events and changes that may influence depressed moods include (but are not limited to): childbirth, menopause, financial difficulties, unemployment, stress (such as from work, education, family, living conditions etc.), a medical diagnosis (cancer, HIV, etc.), bullying, loss of a loved one, natural disasters, social isolation, rape, relationship troubles, jealousy, separation, or catastrophic injury. Adolescents may be especially prone to experiencing a depressed mood following social rejection, peer pressure, or bullying.

Personality

Changes in personality or in one’s social environment can affect levels of depression. High scores on the personality domain neuroticism make the development of depressive symptoms as well as all kinds of depression diagnoses more likely, and depression is associated with low extraversion. Other personality indicators could be: temporary but rapid mood changes, short term hopelessness, loss of interest in activities that used to be of a part of one’s life, sleep disruption, withdrawal from previous social life, appetite changes, and difficulty concentrating.

Medical Treatment

Depression may also be the result of healthcare, such as with medication induced depression. Therapies associated with depression include interferon therapy, beta-blockers, isotretinoin, contraceptives, cardiac agents, anticonvulsants, antimigraine drugs, antipsychotics, and hormonal agents such as gonadotropin-releasing hormone agonist.

Substance-Induced

Several drugs of abuse can cause or exacerbate depression, whether in intoxication, withdrawal, and from chronic use. These include alcohol, sedatives (including prescription benzodiazepines), opioids (including prescription pain killers and illicit drugs such as heroin), stimulants (such as cocaine and amphetamines), hallucinogens, and inhalants.

Non-Psychiatric Illnesses

Refer to Differential Diagnoses of Depression.

Depressed mood can be the result of a number of infectious diseases, nutritional deficiencies, neurological conditions, and physiological problems, including hypoandrogenism (in men), Addison’s disease, Cushing’s syndrome, hypothyroidism, hyperparathyroidism, Lyme disease, multiple sclerosis, Parkinson’s disease, chronic pain, stroke, diabetes, and cancer.

Psychiatric Syndromes

Refer to Depressive Mood Disorders.

A number of psychiatric syndromes feature depressed mood as a main symptom. The mood disorders are a group of disorders considered to be primary disturbances of mood. These include major depressive disorder (MDD; commonly called major depression or clinical depression) where a person has at least two weeks of depressed mood or a loss of interest or pleasure in nearly all activities; and dysthymia, a state of chronic depressed mood, the symptoms of which do not meet the severity of a major depressive episode.

Another mood disorder, bipolar disorder, features one or more episodes of abnormally elevated mood, cognition, and energy levels, but may also involve one or more episodes of depression. When the course of depressive episodes follows a seasonal pattern, the disorder (major depressive disorder, bipolar disorder, etc.) may be described as a seasonal affective disorder.

Outside the mood disorders: borderline personality disorder often features an extremely intense depressive mood; adjustment disorder with depressed mood is a mood disturbance appearing as a psychological response to an identifiable event or stressor, in which the resulting emotional or behavioural symptoms are significant but do not meet the criteria for a major depressive episode; and posttraumatic stress disorder, a mental disorder that sometimes follows trauma, is commonly accompanied by depressed mood.

Historical Legacy

Refer to Dispossession, Oppression and Depression.

Researchers have begun to conceptualise ways in which the historical legacies of racism and colonialism may create depressive conditions.

Measures of Depression

Measures of depression as an emotional disorder include (but are not limited to) the Beck Depression Inventory-11 and the 9-item depression scale in the Patient Health Questionnaire.

Both of these measures are psychological tests that ask personal questions of the participant, and have mostly been used to measure the severity of depression. The Beck Depression Inventory (BDI) is a self-report scale that helps a therapist identify the patterns of depression symptoms and monitor recovery. The responses on this scale can be discussed in therapy to devise interventions for the most distressing symptoms of depression. Several studies, however, have used these measures to also determine healthy individuals who are not suffering from depression as a mental disorder, but as an occasional mood disorder. This is substantiated by the fact that depression as an emotional disorder displays similar symptoms to minimal depression and low levels of mental disorders such as major depressive disorder; therefore, researchers were able to use the same measure interchangeably. In terms of the scale, participants scoring between 0-13 and 0-4 respectively were considered healthy individuals.

Another measure of depressed mood would be the IWP Multi-affect Indicator. It is a psychological test that indicates various emotions, such as enthusiasm and depression, and asks for the degree of the emotions that the participants have felt in the past week. There are studies that have used lesser items from the IWP Multi-affect Indicator which was then scaled down to daily levels to measure the daily levels of depression as an emotional disorder.

Connections

Alcoholism

Alcohol can be a depressant which slows down some regions of the brain, like the prefrontal and temporal cortex, negatively affecting rationality and memory. It also lowers the level of serotonin in the brain, which could potentially lead to higher chances of depressive mood.

The connection between the amount of alcohol intake, level of depressed mood, and how it affects the risks of experiencing consequences from alcoholism, were studied in a research done on college students. The study used 4 latent, distinct profiles of different alcohol intake and level of depression; Mild or Moderate Depression, and Heavy or Severe Drinkers. Other indicators consisting of social factors and individual behaviours were also taken into consideration in the research. Results showed that the level of depression as an emotion negatively affected the amount of risky behaviour and consequence from drinking, while having an inverse relationship with protective behavioural strategies, which are behavioural actions taken by oneself for protection from the relative harm of alcohol intake. Having an elevated level of depressed mood does therefore lead to greater consequences from drinking.

Bullying

Social abuse, such as bullying, are defined as actions of singling out and causing harm on vulnerable individuals. In order to capture a day-to-day observation of the relationship between the damaging effects of social abuse, the victim’s mental health and depressive mood, a study was conducted on whether individuals would have a higher level of depressed mood when exposed to daily acts of negative behaviour. The result concluded that being exposed daily to abusive behaviours such as bullying has a positive relationship to depressed mood on the same day.

The study has also gone beyond to compare the level of depressive mood between the victims and non-victims of the daily bullying. Although victims were predicted to have a higher level of depressive mood, the results have shown otherwise that exposure to negative acts has led to similar levels of depressive mood, regardless of the victim status. The results therefore have concluded that bystanders and non-victims feel as equally depressed as the victim when being exposed to acts such as social abuse.

Creative Thinking

Divergent thinking is defined as a thought process that generates creativity in ideas by exploring many possible solutions. Having a depressed mood will significantly reduce the possibility of divergent thinking, as it reduces the fluency, variety and the extent of originality of the possible ideas generated.

However, some depressive mood disorders might have a positive effect for creativity. Upon identifying several studies and analysing data involving individuals with high levels of creativity, Christa Taylor was able to conclude that there is a clear positive relationship between creativity and depressive mood. A possible reason is that having a low mood could lead to new ways of perceiving and learning from the world, but it is unable to account for certain depressive disorders. The direct relationship between creativity and depression remains unclear, but the research conducted on this correlation has shed light that individuals who are struggling with a depressive disorder may be having even higher levels of creativity than a control group, and would be a close topic to monitor depending on the future trends of how creativity will be perceived and demanded.

Stress Management Techniques

There are empirical evidences of a connection between the type of stress management techniques and the level of daily depressive mood.

Problem-focused coping leads to lower level of depression. Focusing on the problem allows for the subjects to view the situation in an objective way, evaluating the severity of the threat in an unbiased way, thus it lowers the probability of having depressive responses. On the other hand, emotion-focused coping promotes a depressed mood in stressful situations. The person has been contaminated with too much irrelevant information and loses focus on the options for resolving the problem. They fail to consider the potential consequences and choose the option that minimises stress and maximises well-being.

Management

Depressed mood may not require professional treatment, and may be a normal temporary reaction to life events, a symptom of some medical condition, or a side effect of some drugs or medical treatments. A prolonged depressed mood, especially in combination with other symptoms, may lead to a diagnosis of a psychiatric or medical condition which may benefit from treatment. The UK National Institute for Health and Care Excellence (NICE) 2009 guidelines indicated that antidepressants should not be routinely used for the initial treatment of mild depression, because the risk-benefit ratio is poor. Physical activity can have a protective effect against the emergence of depression.

Physical activity can also decrease depressive symptoms due to the release of neurotrophic proteins in the brain that can help to rebuild the hippocampus that may be reduced due to depression. Also yoga could be considered an ancillary treatment option for patients with depressive disorders and individuals with elevated levels of depression.

Reminiscence of old and fond memories is another alternative form of treatment, especially for the elderly who have lived longer and have more experiences in life. It is a method that causes a person to recollect memories of their own life, leading to a process of self-recognition and identifying familiar stimuli. By maintaining one’s personal past and identity, it is a technique that stimulates people to view their lives in a more objective and balanced way, causing them to pay attention to positive information in their life stories, which would successfully reduce depressive mood levels.

Self-help books are a growing form of treatment for peoples physiological distress. There may be a possible connection between consumers of unguided self-help books and higher levels of stress and depressive symptoms. Researchers took many factors into consideration to find a difference in consumers and non-consumers of self-help books. The study recruited 32 people between the ages of 18 and 65; 18 consumers and 14 non-consumers, in both groups 75% of them were female. Then they broke the consumers into 11 who preferred problem-focused and 7 preferred growth-oriented. Those groups were tested for many things including cortisol levels, depressive symptomatology, and stress reactivity levels. There were no large differences between consumers of self-help books and non-consumers when it comes to diurnal cortisol level, there was a large difference in depressive symptomatology with consumers having a higher mean score. The growth-oriented group has higher stress reactivity levels than the problem-focused group. However, the problem-focused group shows higher depressive symptomatology.

Schizophrenia & Smoking Traits

Research Paper Title

Colocalisation of association signals at nicotinic acetylcholine receptor genes between schizophrenia and smoking traits.

Background

Epidemiological data suggest that smoking may be a risk factor for schizophrenia (SCZ), but more evidence is needed. Two regions coding nicotinic acetylcholine receptor (nAchR) subunits, atCHRNA2 and the CHRNA5/A3/B4 cluster, were associated with SCZ in genome-wide association studies (GWAS). Additionally, a signal at CHRNA4 is near significance. CHRNA2 was also associated with cannabis use disorder (CUD). These regions were also associated with smoking behaviours. If tobacco is a risk factor, the GWAS signals at smoking behaviours and SCZ have to be due to the same causal variants, i.e. they have to colocalise, although colocalisation does not necessarily imply causality. Here, we present colocalisation analysis at these loci between SCZ and smoking behaviours.

Methods

The Bayesian approach implemented in coloc was used to check for posterior probability of colocalisation versus independent signals at the three loci with some evidence of association with SCZ and smoking behaviours, using GWAS summary statistics. Colocalisation was also assessed for positive control traits and CUD. Three different sensibility analyses were used to confirm the results. A visualisation tool, LocusCompare, was used to facilitate interpretation of the coloc results.

Results

Evidence for colocalisation of GWAS signals between SCZ and smoking behaviours was found for CHRNA2. Evidence for independent causal variants was found for the other two loci. CUD GWAS signal at CHRNA2 colocalises with SCZ and smoking behaviours.

Conclusions

Overall, the results indicate that the association between some nAchR subunit genes and SCZ cannot be solely explained by their effect on smoking behaviours.

Reference

Al-Soufi, L. & Costas, J. (2021) Colocalization of association signals at nicotinic acetylcholine receptor genes between schizophrenia and smoking traits. Drug and Alcohol Dependence. doi: 10.1016/j.drugalcdep.2021.108517. Online ahead of print.

On This Day … 22 January

People (Births)

  • 1913 – Henry Bauchau, Belgian psychoanalyst and author (d. 2012).
  • 1932 – Berthold Grünfeld, Norwegian psychiatrist and academic (d. 2007).

Henry Bauchau

Henry Bauchau (22 January 1913 to 21 September 2012) was a Belgian psychoanalyst, lawyer, and author of French prose and poetry.

He became a trial lawyer in Brussels in 1936 and was a member of the Belgian Resistance in the Ardennes during World War II.

Berthold Grunfeld

Berthold Grünfeld (22 January 1932 to 20 August 2007) was a Norwegian psychiatrist, sexologist, and professor of social medicine at the University of Oslo. He was also a recognised expert in forensic psychiatry, often employed by Norwegian courts to examine insanity defence pleas.

Grünfeld was born in Bratislava in what was then Czechoslovakia. In 1939, when he was seven, he and 34 other Jewish children were separated from their families in an attempt by Nansenhjelpen to rescue them from the early manifestations of the Holocaust. The group of children was sent by train to Norway via Berlin, after having been told they would never again see their parents.

Once in Norway, Grünfeld was first placed at the Jewish children’s home in Oslo, then lived as a foster child with a Jewish family in Trondheim before returning to the orphanage. During the occupation of Norway, Grünfeld avoided capture and deportation by fleeing with members of the Norwegian Resistance in 1942 to neutral Sweden, where he stayed until the war ended. He returned to the children’s home in 1946. The Jewish community funded his education.

Berthold Grünfeld earned his medical degree in 1960, when he also met his future wife Gunhild. He was awarded his doctorate in medicine in 1973 based on a dissertation on abortion. In 1993, he was made professor of social medicine at the University of Oslo.

Grünfeld was noted for his academic contributions within sexology, on the issues of abortion and euthanasia, and within forensic psychology. In addition to his advocacy and teaching, he acted as an expert witness in criminal cases, and as a consultant on human relations and sexology for Oslo Helseråd. His dissertation influenced the reform of abortion laws in Norway.

Grünfeld and his wife had three children and six grandchildren. In 2005, his daughter Nina Grünfeld made a film, Origin Unknown, about her efforts to research her father’s background and heritage. Among other things, she found that his mother had worked as a prostitute and was murdered in the death camp at Sobibor.

What Skills & Abilities are Required for Peer Support?

Introduction

Peer support is an important element in an individual’s journey as they cope/manage/live with their mental health condition.

Although there is currently only a small research base on the value and effectiveness of peer support, this research is generally positive regarding its impact on the individual (Gillard et al., 2013; Gillard & Holley, 2018):

  • Receiving the peer support (helpee); and
  • Providing the peer support (helper).

Look here for an overview of Peer Support.

This article refers to peer support within the UK, and particularly Scotland (where I live).

Background

Peer support roles are still relatively new in the UK and these exciting new(ish) roles have been developed specifically for individuals who have lived experience of recovery from mental distress.

“An increasing number of organisations and services are developing peer support roles. There are now around 80 paid posts in mental health services and a far higher number of unpaid roles.” (Christie, 2016, p.3).

Within the public sector (i.e. NHS), peer support is a paid role and within the third (charity) sector the role may be paid (i.e. member of staff) or unpaid (i.e. volunteer).

Titles vary also, for example peer worker, peer support worker, peer support specialist, and community support worker.

For administrative purposes, individuals are referred to as Service Users by charities and as Patients by the NHS.

The Role of Peer Support

The overarching purpose of the role is to provide support and assistance to individuals to promote independence and self responsibility. And, as such, you will work alongside existing mental health services to promote and deliver support which facilitates recovery for the individual (it is important to note that recovery means different things to different individuals, i.e. it is a unique process).

Within the role you may be expected to:

  • Use the knowledge gained through your own lived experience to inspire hope and belief that recovery is possible in others.
  • Work with a Community Mental Health Team alongside a clinical team to help patients/service users achieve their recovery goals.
    • To assist individuals to create their own outcomes focused recovery plans.
  • Work with people with complex psychological needs, meaning you will need to be emotionally and mentally resilient.
  • Provide 1:1 and/or group support, exploring the individual’s hopes for moving out of social isolation and towards meaningful opportunities, relationships and community engagement.
  • Draw upon your experiences of recovery and attend training on the most effective way to so this.
  • Be involved in contributing to the development of the peer support role, within mental health services.
  • Develop (and within) a relationship of mutuality and information sharing, promote recovery, self-management and opportunities for improved health and wellbeing.
    • Develop relationships with people based on the principals of peer support.
  • To share ideas about ways of achieving recovery goals, drawing on personal experiences and a range of coping, self help and self-management techniques.
  • Make a positive contribution to the reduction in stigma associated with mental health issues.
  • To model personal responsibility, self-awareness, self-belief, self advocacy and hopefulness.
  • Maintain a working knowledge of current trends in mental health, recovery and peer support through a variety of sources.
    • For example, by reading books, journals and accessing peer support networks.
  • Deal with sensitive and confidential information, and take account of safeguarding and child safety issues.
    • The peer supported should be wary of issues that may bring them into conflict with the patient/service user.
    • Maintain a positive therapeutic relationship and maintain child protection standards.
  • Work in partnership with other organisations.

Purpose of the Role

The exact provision of support will vary between organisations, and the following examples are for illustration only.

Example 01

  • Building supportive and respectful relationships with patients on the ward/service users in the charity.
  • Supporting others using the personal experience and confidence you have gained having overcome similar challenges.
  • Assisting clinical/charity staff to help people identify their own recovery goals.
  • Providing information and support to family and friends of patients/service users.
  • Developing the peer support worker programme and role within organisation.
  • Modelling personal responsibility, self-awareness, self-belief, self-advocacy and hopefulness.

Example 02

  • Wellbeing mentors will take a lead in delivering all one to one therapeutic and group work activity. They will also provide one to one support and key-working interventions using Wellness Recovery Action Plans.
  • Building and developing service users’ personal strengths, social networks and recovery capital (social, physical, human and cultural).
  • Provide practical support and supervision to volunteers/ Peer Workers as required.
  • Develop effective relationships with other groups and agencies in our area and take opportunities to promote mental health awareness in the wider community.
  • Effectively and proactively connecting service users into a range of health and social care services that support their recovery.
  • To assist the Lead Practitioner in addressing clients support needs and to review progress with clients at regular intervals.
  • To participate in effective team work and establish good channels of communication to all local organisations.
  • To promote peer and volunteering opportunities within the service.
  • To provide an efficient and welcoming reception service to visitors to the unit.

From the above two examples, we can see that peer support may offer a range of services that provide practical, emotional and social support. And, these services should be focused on improving health and wellbeing and aim to ensure that all the services are flexible, personalised and recovery focused.

What Attitude/Skills/Knowledge Do You Need for the Role of Peer Support?

  • A background of personally recovering from mental health issues.
  • Past and lived experience of using mental health services or awareness of mental health issues.
  • An understanding of the impact of mental health issues on individuals, families, and communities.
  • Resilience and to be able to know when to ask for help.
  • Demonstrate an awareness of mental health interventions and commitment to supporting recovery.
  • An understanding of factors which can affect recovery in mental health.
  • IT literacy including Microsoft Office and Internet or a willingness to learn.
  • Strong verbal and written communication skills.
  • The ability to work well in a multi-disciplinary team.
  • Empathy, good listening skills, approach-ability and common sense.
  • Enthusiastic, motivated, and positive in outlook.

Support for the Peer Support Role

For those in the NHS, they will receive formal/structured induction, training and on-going supervision, including a network of other peer support workers employed within the NHS.

Within the charity sector, induction, training, and ongoing supervision varies between organisations.

What is the Most Challenging/Difficult Part of the Role

Experience of what is challenging or difficult will depend on the background of the peer supporter, and below are some examples.

  • Aspects of the role can prove to be mentally demanding and stressful.
  • The peer supporter is required to provide mental effort and concentration due to confidentiality and the sensitivity of information, which is being given and sought.
  • There are emotional demands when communicating with distressed, anxious, worried individuals or relatives.
    • It is necessary to maintain a non-judgemental approach when discussing sensitive issues.
  • The peer supporter will have lived experience of mental health issues.
    • It is necessary for the peer supporter to demonstrate the ability to take personal responsibility with regards to their own personal recovery needs, limitations and support needs.
  • To assist members of staff/volunteers in providing comprehensive recovery focussed support to individuals who have a range of physical, mental and emotional issues and who may display verbal and/or physical aggression.
  • To work with individuals who may have negative preconceptions of health and social care, having had experience of discrimination from other services/organisations/people due to their mental health issue(s).
  • Responding to acute symptoms of relapse and challenging behaviour of individuals in isolated or public locations while unsupervised in the community.
  • Using initiative when alone with individuals in crisis and instigating emergency procedures in conjunction with trained staff.

Useful Courses

There are a number of optional/mandatory courses which a potential peer supporter can attend.

  • Individual Recovery Outcomes Counter (I.ROC).
  • Recovery in Practice.
  • Wellness Recovery Action Planning (WRAP).
  • Recovery & WRAP.
  • Coaching.
  • Personal Planning.
  • Managing Risk.
  • Managing Actual and Potential Aggression.
  • Scottish Mental Health First Aid.
  • Applied Suicide Intervention Skills Training.
  • Mental Health Awareness.
  • Self Harm Awareness.
  • HOPE Toolkit (Home, Opportunity, People, and Empowerment).
  • SVQ 3 in Healthcare (superseded by SVQ 3 Social Services and Healthcare at SCQF Level 7).
    • To work in the NHS you must have a recognised healthcare qualification.
    • This is a work-based course.
    • Can have an equivalent as defined by the Scottish Social Services Council (SSSC).
    • Mandatory to apply for role in some organisations, others state willingness to work towards, and some state relevant previous experience working with individuals who have mental health issues.
  • PDA in Mental Health Peer Support or a relevant course in peer support.
    • Mandatory to apply for role in some organisations, others state willingness to work towards.

Co-Workers

In peer support you will work with a variety of volunteers and professionals in a mix of roles, including:

  • Clinical staff (psychiatrists, psychologists, nurses etc.).
  • Recovery Worker.
  • Recovery Practitioner.
  • Peer Worker.
  • Community Addiction Worker.

Further Reading

References

Christie, L. (2016) Peer Support Roles in Mental Health Services. Available from World Wide Web: https://www.iriss.org.uk/sites/default/files/2016-06/insights-31.pdf. [Accessed: 21 January, 2021].

What is Capgras Delusion?

Introduction

Capgras delusion is a psychiatric disorder in which a person holds a delusion that a friend, spouse, parent, or other close family member (or pet) has been replaced by an identical impostor. It is named after Joseph Capgras (1873-1950), a French psychiatrist.

The Capgras delusion is classified as a delusional misidentification syndrome, a class of delusional beliefs that involves the misidentification of people, places, or objects. It can occur in acute, transient, or chronic forms. Cases in which patients hold the belief that time has been “warped” or “substituted” have also been reported.

The delusion most commonly occurs in individuals diagnosed with paranoid schizophrenia but has also been seen in brain injury, dementia with Lewy bodies, and other dementia. It presents often in individuals with a neurodegenerative disease, particularly at an older age. It has also been reported as occurring in association with diabetes, hypothyroidism, and migraine attacks. In one isolated case, the Capgras delusion was temporarily induced in a healthy subject by the drug ketamine. It occurs more frequently in females, with a female to male ratio of approximately 3 to 2.

Signs and Symptoms

The following two case reports are examples of the Capgras delusion in a psychiatric setting:

Example 01

Mrs. D, a 74-year-old married housewife, recently discharged from a local hospital after her first psychiatric admission, presented to our facility for a second opinion. At the time of her admission earlier in the year, she had received the diagnosis of atypical psychosis because of her belief that her husband had been replaced by another unrelated man. She refused to sleep with the impostor, locked her bedroom and door at night, asked her son for a gun, and finally fought with the police when attempts were made to hospitalise her. At times she believed her husband was her long deceased father. She easily recognised other family members and would misidentify her husband only.

Example 02

Diane was a 28-year-old single woman who was seen for an evaluation at a day hospital program in preparation for discharge from a psychiatric hospital. This was her third psychiatric admission in the past five years. Always shy and reclusive, Diane first became psychotic at age 23. Following an examination by her physician, she began to worry that the doctor had damaged her internally and that she might never be able to become pregnant. The patient’s condition improved with neuroleptic treatment but deteriorated after discharge because she refused medication. When she was admitted eight months later, she presented with delusions that a man was making exact copies of people—”screens”—and that there were two screens of her, one evil and one good. The diagnosis was schizophrenia with Capgras delusion. She was disheveled and had a bald spot on her scalp from self-mutilation.

Example 03

The following case is an instance of the Capgras delusion resulting from a neurodegenerative disease:

Fred, a 59-year-old man with a high school qualification, was referred for neurological and neuropsychological evaluation because of cognitive and behavioural disturbances. He had worked as the head of a small unit devoted to energy research until a few months before. His past medical and psychiatric history was uneventful. […] Fred’s wife reported that about 15 months from onset he began to see her as a “double” (her words). The first episode occurred one day when, after coming home, Fred asked her where Wilma was. On her surprised answer that she was right there, he firmly denied that she was his wife Wilma, whom he “knew very well as his sons’ mother”, and went on plainly commenting that Wilma had probably gone out and would come back later. […] Fred presented progressive cognitive deterioration characterised both by severity and fast decline. Apart from [Capgras disorder], his neuropsychological presentation was hallmarked by language disturbances suggestive of frontal-executive dysfunction. His cognitive impairment ended up in a severe, all-encompassing frontal syndrome.

Causes

It is generally agreed that the Capgras delusion has a complex and organic basis caused by structural damage to organs and can be better understood by examining neuroanatomical damage associated with the syndrome.

In one of the first papers to consider the cerebral basis of the Capgras delusion, Alexander, Stuss and Benson pointed out in 1979 that the disorder might be related to a combination of frontal lobe damage causing problems with familiarity and right hemisphere damage causing problems with visual recognition.

Further clues to the possible causes of the Capgras delusion were suggested by the study of brain-injured patients who had developed prosopagnosia. In this condition, patients are unable to recognise faces consciously, despite being able to recognise other types of visual objects. However, a 1984 study by Bauer showed that even though conscious face recognition was impaired, patients with the condition showed autonomic arousal (measured by a galvanic skin response measure) to familiar faces, suggesting that there are two pathways to face recognition – one conscious and one unconscious.

In a 1990 paper published in the British Journal of Psychiatry, psychologists Hadyn Ellis and Andy Young hypothesized that patients with Capgras delusion may have a “mirror image” or double dissociation of prosopagnosia, in that their conscious ability to recognise faces was intact, but they might have damage to the system that produces the automatic emotional arousal to familiar faces. This might lead to the experience of recognising someone while feeling something was not “quite right” about them. In 1997, Ellis and his colleagues published a study of five patients with Capgras delusion (all diagnosed with schizophrenia) and confirmed that although they could consciously recognise the faces, they did not show the normal automatic emotional arousal response. The same low level of autonomic response was shown in the presence of strangers. Young (2008) has theorised that this means that patients with the disease experience a “loss” of familiarity, not a “lack” of it. Further evidence for this explanation comes from other studies measuring galvanic skin responses (GSR) to faces. A patient with Capgras delusion showed reduced GSRs to faces in spite of normal face recognition. This theory for the causes of Capgras delusion was summarised in Trends in Cognitive Sciences in 2001.

William Hirstein and Vilayanur S. Ramachandran reported similar findings in a paper published on a single case of a patient with Capgras delusion after brain injury. Ramachandran portrayed this case in his book Phantoms in the Brain[24] and gave a talk about it at TED 2007. Since the patient was capable of feeling emotions and recognising faces but could not feel emotions when recognising familiar faces, Ramachandran hypothesizes that the origin of Capgras syndrome is a disconnection between the temporal cortex, where faces are usually recognised, and the limbic system, involved in emotions. More specifically, he emphasizes the disconnection between the amygdala and the inferotemporal cortex.

In 2010, Hirstein revised this theory to explain why a person with Capgras syndrome would have the particular reaction of not recognizing a familiar person. Hirstein explained the theory as follows:

My current hypothesis on Capgras, which is a more specific version of the earlier position I took in the 1997 article with V. S. Ramachandran. According to my current approach, we represent the people we know well with hybrid representations containing two parts. One part represents them externally: how they look, sound, etc. The other part represents them internally: their personalities, beliefs, characteristic emotions, preferences, etc. Capgras syndrome occurs when the internal portion of the representation is damaged or inaccessible. This produces the impression of someone who looks right on the outside, but seems different on the inside, i.e., an impostor. This gives a much more specific explanation that fits well with what the patients actually say. It corrects a problem with the earlier hypothesis in that there are many possible responses to the lack of an emotion upon seeing someone.

Furthermore, Ramachandran suggests a relationship between the Capgras syndrome and a more general difficulty in linking successive episodic memories because of the crucial role emotion plays in creating memories. Since the patient could not put together memories and feelings, he believed objects in a photograph were new on every viewing, even though they normally should have evoked feelings (e.g. a person close to him, a familiar object, or even himself). Others like Merrin and Silberfarb (1976) have also proposed links between the Capgras syndrome and deficits in aspects of memory. They suggest that an important and familiar person (the usual subject of the delusion) has many layers of visual, auditory, tactile, and experiential memories associated with them, so the Capgras delusion can be understood as a failure of object constancy at a high perceptual level.

Most likely, more than just an impairment of the automatic emotional arousal response is necessary to form the Capgras delusion, as the same pattern has been reported in patients showing no signs of delusions. Ellis suggested that a second factor explains why this unusual experience is transformed into a delusional belief; this second factor is thought to be an impairment in reasoning, although no definitive impairment has been found to explain all cases. Many have argued for the inclusion of the role of patient phenomenology in explanatory models of the Capgras syndrome in order to better understand the mechanisms that enable the creation and maintenance of delusional beliefs.

Capgras syndrome has also been linked to reduplicative paramnesia, another delusional misidentification syndrome in which a person believes a location has been duplicated or relocated. Since these two syndromes are highly associated, it has been proposed that they affect similar areas of the brain and therefore have similar neurological implications. Reduplicative paramnesia is understood to affect the frontal lobe, and thus it is believed that Capgras syndrome is also associated with the frontal lobe. Even if the damage is not directly to the frontal lobe, an interruption of signals between other lobes and the frontal lobe could result in Capgras syndrome.

Diagnosis

Because it is a rare and poorly understood condition, there is no definitive way to diagnose the Capgras delusion. Diagnosis is primarily made on a psychiatric evaluation of the patient, who is most likely brought to a psychiatrist’s attention by a family member or friend believed to be an imposter by the person under the delusion.

Treatment

Treatment has not been well studied and so there is no evidence-based approach. Treatment is generally therapy, often with support of antipsychotic medication.

Brief History

Capgras syndrome is named after Joseph Capgras, a French psychiatrist who first described the disorder in 1923 in his paper co-authored by Jean Reboul-Lachaux, on the case of a French woman, “Madame Macabre,” who complained that corresponding “doubles” had taken the places of her husband and other people she knew. Capgras and Reboul-Lachaux first called the syndrome “l’illusion des sosies”, which can be translated literally as “the illusion of look-alikes.”

The syndrome was initially considered a purely psychiatric disorder, the delusion of a double seen as symptomatic of schizophrenia, and purely a female disorder (though this is now known not to be the case) often noted as a symptom of hysteria. Most of the proposed explanations initially following that of Capgras and Reboul-Lachaux were psychoanalytical in nature. It was not until the 1980s that attention was turned to the usually co-existing organic brain lesions originally thought to be essentially unrelated or accidental. Today, the Capgras syndrome is understood as a neurological disorder, in which the delusion primarily results from organic brain lesions or degeneration.

In Popular Culture

In the Memoirs Found in a Bathtub novel by the Polish writer Stanisław Lem, first published in 1961, the narrator inhabits a paranoid dystopia where nothing is as it seems, chaos seems to rule all events, and everyone is deeply suspicious of everyone. In the end, it is revealed that the world is filled by phantom body doubles.

A central character in Richard Powers’s 2006 novel The Echo Maker suffers from Capgras Delusion subsequent to traumatic brain injury.

The protagonist in the movie Synecdoche, New York, who is named Caden Cotard (played by Philip Seymour Hoffman), goes to see his ex-wife at her apartment, and, as he enters the building, one of the resident call boxes is taped with the name “Capgras”. He is then misidentified as his ex-wife’s cleaning lady, Ellen Bascomb, as he tries to enter the apartment, and, later in the film, he actually comes to play the role of Ellen Bascomb in his own play. Throughout the film, Cotard enlists actor-doubles to play actors, and, as the film progresses, the actor-doubles are in turn then given actors-doubles.

In “Dorado Falls,” an episode from the seventh season of the television series Criminal Minds, a Navy SEAL develops Capgras delusion as the result of an automobile accident. His experience with classified military missions causes him to become extremely paranoid, and he begins killing the people he sees on a regular basis, believing them to have been replaced by duplicates who are plotting against him.

Does Lack of a Consistent Definition Hinder Treatment for Clozapine-Resistant Schizophrenia Patients?

Research Paper Title

Characteristics and definitions of ultra-treatment-resistant schizophrenia – A systematic review and meta-analysis.

Background

The aim of this systematic review and meta-analysis was to characterise ultra-treatment-resistant Schizophrenia also known as clozapine-resistant schizophrenia (CRS) patients across clozapine combination and augmentation trials through demographic and clinical baseline data. Furthermore, the researchers investigated the variability and consistency in CRS definitions between studies.

Methods

Systematic searches of articles indexed in PubMed, EMBASE, the Cochrane Central Register of Controlled Trials (CENTRAL) and PsycINFO were conducted in March 2020. 1541 randomised and non-randomised clinical trials investigating pharmacological and non-pharmacological clozapine add-on strategies were screened and a total of 71 studies were included. The primary outcome was the overall symptom score at baseline, measured with Positive and Negative Syndrome Scale (PANSS) total or Brief Psychiatric Rating Scale (BPRS) total scores.

Results

Data from 2731 patients were extracted. Patients were overall moderately ill with a mean PANSS total score at baseline of 79.16 (±7.52), a mean duration of illness of 14.64 (±4.14) years with a mean clozapine dose of 436.94 (±87.47) mg/day. Illness severity data were relatively homogenous among patients independently of the augmentation strategy involved, although stark geographical differences were found. Overall, studies showed a large heterogeneity of CRS definitions and insufficient guidelines implementation.

Conclusions

This first meta-analysis characterising CRS patients and comparing CRS definitions revealed a lack of consistent implementation of a CRS definition from guidelines into clinical trials, compromising the replicability of the results and their applicability in clinical practice. The researchers offer a new score modelled on a best practice definition to help future trials increase their reliability.

Reference

Campana, M., Falkai, P., Siskind, D., Hasan, A. & Wagner, E. (2021) Characteristics and definitions of ultra-treatment-resistant schizophrenia – A systematic review and meta-analysis. Schizophrenia Research. 228, pp.218-226. doi: 10.1016/j.schres.2020.12.002. Online ahead of print.